Mechenical ventilation

The basics of: Invasive positive pressure ventilation (IPPV), Noninvasive positive pressure ventilation (NIPPV)

1. Basics of Basics of
Mechanical VentilationMechanical Ventilation
Sarvodaya Manav Seva Charitable Trust
YOUR NAME
Institute
Share the knowledge! Spread the Health!
PLEASE SEND US THE PRESENTATIONS (PPT), DOC FILES, PDF FILES, PHOTOGRAPHS, VIDEOS etc,
WHICH ARE RELATED TO HEALTH & MEDICAL. WE WILL SHOW THEM AT
www.YouNHealth.Com WITH YOUR NAME.
Email: [email protected],

2. Objectives
How positive pressure ventilation helps ?
•Reduce the work of breathing
•Restore adequate gas exchange
The basics of:
•Invasive positive pressure ventilation (IPPV)
•Noninvasive positive pressure ventilation (NIPPV)
The principles of bedside monitoring
•Pressure and volume alarms
•Flow and pressure time curves
Sarvodaya Manav Seva Charitable Trust

3. Indications and Rationale for Initiating IPPVIndications and Rationale for Initiating IPPV
•Unprotected and unstable airways (e.g. coma) Intubation
and IPPV allows to
-Secure the airways
-Reduce the risk of aspiration
-Maintain adequate alveolar ventilation
•Hypercapnic respiratory acidosis
IPPV and NIPPV
-Reduce the work of breathing and thus prevents respiratory muscle
fatigue or speeds recovery when fatigue is already present
-Maintain adequate alveolar ventilation (prevent or limit respiratory
acidosis as needed)
Sarvodaya Manav Seva Charitable Trust

4. Indications and Rationale for Initiating IPPVIndications and Rationale for Initiating IPPV
Hypoxic respiratory failure
IPPV and NIPPV help correct hypoxemia as it allows to:
•Deliver a high FiO2 (100% if needed during IPPV)
•Reduce shunt by maintaining flooded or collapsed alveoli open
•Others
Intubation to facilitate procedure (bronchoscopy), bronchial suctioning
Sarvodaya Manav Seva Charitable Trust

5. Pitfalls and Problems Associated with PPV Pitfalls and Problems Associated with PPV
Potential detrimental effects associated with PPV
●Heart and circulation
-Reduced venous return and afterload
-Hypotension and reduced cardiac output
●Lungs
-Barotrauma
-Ventilator-induced lung injury
-Air trapping
●Gas exchange
-May increase dead space (compression of capillaries)
-Shunt (e.g., unilateral lung disease - the increase in vascular resistance in the
normal lung associated with PPV tends to redirect blood flow in the abnormal
lung)
Sarvodaya Manav Seva Charitable Trust

6. Decreased preload
●Positive alveolar pressure  ↑ lung volume  compression of the
heart by the inflated lungs  the intramural pressure of the heart
cavities rises (e.g., ↑ RAP)  venous return decreases  preload is
reduced  stroke volume decreases  cardiac output and blood
pressure may drop. This can be minimized with i.v. fluid, which helps
restore adequate venous return and preload.
●Patients who are very sensitive to change in preload conditions (e.g.,
presence of hypovolemia, tamponade, PE, severe air trapping) are
particularly prone to hypotension when PPV is initiated.
Important Effects of PPV on HemodynamicsImportant Effects of PPV on Hemodynamics
Sarvodaya Manav Seva Charitable Trust

7. Reduced afterload
●
Lung expansion increases extramural pressure (which helps pump
blood out of the thorax) and thereby reduces LV afterload.
●
When the cardiac performance is mainly determined by changes in
afterload than in preload conditions (e.g., hypervolemic patient with
systolic heart failure), PPV may be associated with an improved stroke
volume. PPV is very helpful in patients with cardiogenic pulmonary
edema, as it helps to reduce preload (lung congestion) and afterload.
As a result stroke volume tends to increase.
Important Effects of PPV on HemodynamicsImportant Effects of PPV on Hemodynamics
Sarvodaya Manav Seva Charitable Trust

8. Other Potentially Adverse Effects of Mechanical Other Potentially Adverse Effects of Mechanical
Ventilation Ventilation
Excessive airway pressure and tidal volume can lead to lung injury (ventilator
induced lung injury) and contribute to increased mortality.
The Acute Respiratory Distress Syndrome
Network. N Engl J Med. 2000;342:1301-1308.
Lungs of dogs ventilated for a few hours with large tidal
volume demonstrate extensive hemorrhagic injury.
Sarvodaya Manav Seva Charitable Trust

9. Other Potentially Adverse Effects of Mechanical Other Potentially Adverse Effects of Mechanical
Ventilation Ventilation
In the setting of obstructive physiology (e.g., asthma and COPD), adjustment of the tidal
volume and rate minute ventilation to restore a normal pH and PaCO
2 can lead to air
trapping, pneumothoraces, and severe hypotension.
Tuxen et al. Am Rev Resp Dis 1987;136:872.
When airway resistances are high, for a few
breath more air going in than coming out
of the lungs (dynamic hyperinflation).
Subsequently, a new equilibrium is
reached. (Upper Panel)
The amount of air trapped can be estimated in
a passive patient by discontinuing
ventilation and collecting the expired
volume (Lower panel).
Sarvodaya Manav Seva Charitable Trust

10. Work of BreathingWork of Breathing
•Work per breath is depicted as a pressure-volume area
•Work per breath (W
breath
)

= P x tidal volume

(V
T
)
•W
min
= w
breath
x respiratory rate
Pressure Pressure Pressure
Volume Volume Volume
V
T
W
R
= resistive
work
W
EL
= elastic
work
The total work of breathing can be partitioned between an elastic and resistive work. By analogy, the pressure needed to
inflate a balloon through a straw varies; one needs to overcome the resistance of the straw and the elasticity of the balloon.
Sarvodaya Manav Seva Charitable Trust

11. Intrinsic PEEP and Work of Breathing Intrinsic PEEP and Work of Breathing
Volume
V
T
V
T
FRC
Pressure
PEEPi
Dynamic
Hyperinflation
PEEPi = intrinsic or auto PEEP; green triangle = tidal elastic work; red loop = flow resistive work; blue rectangle = work
expended in offsetting intrinsic PEEP (an expiratory driver) during inflation
When present, intrinsic PEEP contributes to the work of breathing
and can be offset by applying external PEEP.
Sarvodaya Manav Seva Charitable Trust

12. The Pressure and Work of Breathing can be Entirely The Pressure and Work of Breathing can be Entirely
Provided by the Ventilator (Passive Patient)Provided by the Ventilator (Passive Patient)
+
+
+
+
Ventilator
₊
₊
Sarvodaya Manav Seva Charitable Trust

13. The Work of Breathing can be Shared Between the The Work of Breathing can be Shared Between the
Ventilator and the Patient Ventilator and the Patient
The ventilator generates positive pressure within the airway and the patient’s
inspiratory muscles generate negative pressure in the pleural space.
P
AW
P
ES
patientmachine
time
AC mode
Paw = Airway pressure, Pes= esophageal pressure Sarvodaya Manav Seva Charitable Trust

14. Partitioning of the Workload Between the Ventilator and Partitioning of the Workload Between the Ventilator and
the Patientthe Patient
How the work of breathing partitions
between the patient and the ventilator
depends on:
●
Mode of ventilation (e.g., in assist
control most of the work is usually done
by the ventilator)
●
Patient effort and synchrony with
the mode of ventilation
●
Specific settings of a given mode
(e.g., level of pressure in PS and set
rate in SIMV)
Sarvodaya Manav Seva Charitable Trust

15. Common Modes of VentilationCommon Modes of Ventilation
Volume targeted ventilation (flow controlled, volume cycled)
•AC
Pressure targeted ventilation
•PCV (pressure controlled, time cycled)
•PS
Combination modes
•SIMV with PS and either volume or pressure-targeted mandatory cycles
Sarvodaya Manav Seva Charitable Trust

16. Pressure and Volume Targeted Ventilation Pressure and Volume Targeted Ventilation
•Pressure and volume targeted ventilation obey the same principles set by
the equation of motion.
•In pressure-targeted ventilation: an airway pressure target and inspiratory
time are set, while flow and tidal volume become the dependent variables.
In volume targeted ventilation (flow-controlled, volume cycled), a target
volume and flow (or inspiratory time in certain ventilator) are preset and
pressure and inspiratory time (or flow in the ventilator where inspiratory
time is preset) become the dependent variables.
The tidal volume is the integral of the flow during inspiration = area under
the curve of the flow time curve during inspiration (see next slide).
Sarvodaya Manav Seva Charitable Trust

17. Pressure and Volume Targeted Ventilation Pressure and Volume Targeted Ventilation
Marini, Wheeler. Crit Care Med. The Essentials. 1997.
VT
Sarvodaya Manav Seva Charitable Trust

18. Assist-controlAssist-control
Set variables
•Volume, T
I
or flow rate, frequency, flow profile (constant or decel)
•PEEP and FIO
2
Mandatory breaths
•Ventilator delivers preset volume and preset flow rate at a set back-up rate
Spontaneous breaths
•Additional cycles can be triggered by the patient but otherwise are identical to the
mandatory breath.
Sarvodaya Manav Seva Charitable Trust

19. SIMVSIMV
Key set variables
•Targeted volume (or pressure target), flow rate (or inspiratory time, Ti), mandated frequency
•PEEP, FIO
2
, pressure support
Mandatory breaths
•Ventilator delivers a fixed number of cycles with a preset volume at preset flow rate.
Alternatively, a preset pressure is applied for a specified Ti
Spontaneous breaths
•Unrestricted number, aided by the selected level of pressure support
Sarvodaya Manav Seva Charitable Trust

20. Pressure Controlled VentilationPressure Controlled Ventilation
•Key set variables:
•Pressure, T
I
, and frequency
•PEEP and FIO
2

Mandatory breaths
•Ventilator generates a predetermined pressure for a preset time
Spontaneous breaths
•PCV-AC mode: same as mandatory breaths
•PCV-SIMV mode: unsupported or PS
Important caveat
•Above a certain frequency (e.g., when intrinsic PEEP is created due to a reduced expiratory
time), the driving pressure (set PC pressure – PEEPtotal) starts to drop--and so does the
delivered tidal volume.
•A pneumothorax or other adverse change in the mechanics of the respiratory system will not
trigger a high alarm pressure but a low tidal volume alarm instead.
Sarvodaya Manav Seva Charitable Trust

21. Pressure SupportPressure Support
Pressure = set variable.
Mandatory breaths: none.
Spontaneous breaths
•Ventilator provides a preset pressure assist, which terminates when flow drops
to a specified fraction (typically 25%) of its maximum.
•Patient effort determines size of breath and flow rate.
Sarvodaya Manav Seva Charitable Trust

22. Auto-PEEP (Intrinsic PEEP, PEEPi)Auto-PEEP (Intrinsic PEEP, PEEPi)
Marini, Wheeler. Crit Care Med. The Essentials. 1997.
Note that AutoPEEP is not equivalent to air trapping. Active expiratory muscle contraction is an often under appreciated
contributor (left panel) to positive pressure at the end of expiration
Sarvodaya Manav Seva Charitable Trust

23. Suspecting and Measuring AutoPEEP Suspecting and Measuring AutoPEEP
Suspect AutoPEEP if flow at the end of expiration does not return to the zero baseline.
AutoPEEP is commonly measured by performing a pause at the end of expiration. In a passive patient, flow interruption is
associated with pressure equilibration through the entire system. In such conditions, proximal airway pressure tracks the mean
alveolar pressure caused by dynamic hyperinflation.
Time
Pressure
PEEPe
PEEPi
Total PEEP
End expiratory pause
Sarvodaya Manav Seva Charitable Trust

24. Mechanical Ventilation and Gas Mechanical Ventilation and Gas
ExchangeExchange
Respiratory acidosis
Hypoxemia
Sarvodaya Manav Seva Charitable Trust

25. Hypercapnic AcidosisHypercapnic Acidosis
•Determinants of PaCO
2
•PACO
2
= 0.863 x VCO
2
/VA
•VA = VE (1-VD/VT)
•
Causes of hypercapnia
•Inadequate minute ventilation (VE)
•Dead space ventilation ­ (VD/VT)
•CO
2
production ­ (VCO
2
)
Corrective measures for respiratory acidosis
•When appropriate, increase the minute ventilation (e.g., the rate or the
tidal volume )
VD = dead space
VA = alveolar ventilation
VE = minute ventilation
VT = tidal volume
VCO2 = CO2
production
Sarvodaya Manav Seva Charitable Trust

26. Mechanism for Arterial HypoxemiaMechanism for Arterial Hypoxemia
•Reduced FiO
2
(e.g., toxic fumes, altitude)
Hypoventilation
Impaired diffusion
•Ventilation/perfusion (V
A
/Q) mismatching
•High V
A
/Q
•Low V
A/Q
Shunting
•If significant shunting is present, the FIO2 requirement is typically > 60%
Sarvodaya Manav Seva Charitable Trust

27. Approach to MVApproach to MV
Is MV indicated ?
Conservative
treatment and
periodic
reassessment
NO
YES
Contraindication to NIPPV ?
NIPPV
NO
Success ? Invasive MV
YES
NO
YES
Sarvodaya Manav Seva Charitable Trust

28. Noninvasive VentilationNoninvasive Ventilation
Ventilatory support provided without invasive airway control
•No tracheostomy
•No ETT
Sarvodaya Manav Seva Charitable Trust

29. Key Differences Between NIPPV and IPPV Key Differences Between NIPPV and IPPV
Allows the patients to
maintain normal functions
•Speech
•Eating
Helps avoid the risks and
complications related to:
•Intubation
•Sedation
 Less ventilator-associated
pneumonia
Less airway pressure is
tolerated
Does not protect against
aspiration
No access to airway for
suctioning
Advantages of NIPPVAdvantages of NIPPV Disadvantages of NIPPVDisadvantages of NIPPV
Sarvodaya Manav Seva Charitable Trust

30. Clinical Use of NIPPV in Intensive CareClinical Use of NIPPV in Intensive Care
Decompensated COPD (Hypercapnic Respiratory Failure)
Cardiogenic pulmonary edema
Hypoxic respiratory failure
Other possible indications
•Weaning (post-extubation)
•Obesity hypoventilation syndrome
•Patients deemed not to be intubated
•Post-surgery
•Asthma
Adapted from: Am J Respir Crit Care Med. 2001;163:283-291.Sarvodaya Manav Seva Charitable Trust

31. Contraindications to NIPPVContraindications to NIPPV
Cardiac or respiratory arrest
Nonrespiratory organ failure
Severe encephalopathy (e.g., GCS < 10)
Severe upper gastrointestinal bleeding
Hemodynamic instability or unstable cardiac arrhythmia
Facial surgery, trauma, or deformity
Upper airway obstruction
Inability to cooperate/protect the airway
Inability to clear respiratory secretions
High risk for aspiration
Adapted from: Am J Respir Crit Care Med. 2001;163:283-291.Sarvodaya Manav Seva Charitable Trust

32. Initiating NIPPVInitiating NIPPV
•Initial settings:
•Spontaneous trigger mode with backup rate
•Start with low pressures
-IPAP 8 - 12 cmH
2
O
-PEEP 3 - 5 cmH
2
O
•Adjust inspired O
2
to keep O
2
sat > 90%
•Increase IPAP gradually up to 20 cm H
2
O (as tolerated) to:
-alleviate dyspnea
-decrease respiratory rate
-increase tidal volume
-establish patient-ventilator synchrony
Sarvodaya Manav Seva Charitable Trust

33. Success and Failure Criteria for NPPV Success and Failure Criteria for NPPV
•Improvements in pH and PCO
2
occurring within 2 hours predict the eventual
success of NPPV.
If stabilization or improvement has not been achieved during this time
period, the patient should be considered an NPPV failure and intubation
must be strongly considered.
Other criteria for a failed NPPV trial include: worsened encephalopathy or
agitation, inability to clear secretions, inability to tolerate any available mask,
hemodynamic instability, worsened oxygenation.
Sarvodaya Manav Seva Charitable Trust

34. Post Module Testing: Case 1Post Module Testing: Case 1
29-year-old patient (weight 120 kg, height 170 cm)
ARDS secondary to bilateral pneumonia
•Ventilator settings: AC with V
T 800 ml and back-up rate 10/min,
PEEP 5 cmH
2O, FIO
2 80 %
•Measured variables: rate 25, V
E
= 20 l/min, Ppeak 40 cm H
2
O,
Pplat 35 cm H
2
O
•ABG: pH 7.40, PaO
2
55 mmHg, PaCO
2
38 mmHg, O
2
saturation
85%
Sarvodaya Manav Seva Charitable Trust

35. Question 1Question 1
What mechanism best explains the patient’s hypoxemia?
1.V/Q mismatch
2.Shunt
3.Abnormal diffusion
4.Inadequate oxygen delivery and high tissue extraction
Sarvodaya Manav Seva Charitable Trust

36. Answer 1Answer 1
•If in a ventilated patient, FIO
2
> 60% is needed, shunt is
certainly the main cause for the hypoxemia (correct response:
2).
•As a rule, increasing the FIO
2
will compensate for V
A
/Q
mismatching but not for shunt. When V
A
/Q mismatching is
present, hypoxemia typically corrects with an FIO
2
< 60%.
Altered diffusion is rarely a clinically relevant issue.
Increasing the ventilation rate will not exert a significant
impact on oxygenation unless it contributes to air trapping and
auto-PEEP.
Sarvodaya Manav Seva Charitable Trust

37. Question 2Question 2
Which of the following ventilatory setting changes is the next best
step to reduce shunt and increase the PaO
2
/FIO
2
ratio (a
bedside index of oxygen exchange)

–Increase PEEP to 10 cmH
2
0
–Increase the FIO
2 to 100%
–Add an inspiratory pause of 1 second
–Increase respiratory rate to 30/min
Sarvodaya Manav Seva Charitable Trust

38. Answer 2Answer 2
Interventions that target mean airway pressure are the most helpful. They
help recruit flooded or collapsed alveoli and maintain the recruited alveoli
open for gas exchange (reduced shunt).
Increasing PEEP is the first intervention to consider; extending the
inspiratory time and I:E ratio is a secondary option to raise mean airway
pressure.
•In the presence of shunt, increasing the FIO
2 would reduce the ratio.
Although increasing rate may affect meanPaw, its impact is overall minor.
Rate adjustment is mainly used to control minute ventilation and its
consequences on:
•air trapping
•PaCO
2
and pH
Sarvodaya Manav Seva Charitable Trust

39. Question 3Question 3
•PEEP is increased to 10 cmH
2
0
•PaO
2
is now 85 mmHg, Pplat is 45, and Ppeak 50 cmH
2
O
The high pressure alarm is now triggered.
Your next step is:
–Reset the alarm pressure to 55 cmH
20.
–Disconnect the patient from the ventilator and start manual ventilation
(bagging).
–Order a stat chest x-ray to assess for a pneumothorax.
–Reduce the tidal volume slowly until the alarm turns off.
–None of the above
Sarvodaya Manav Seva Charitable Trust

40. Answer 3Answer 3
The correct answer is 5. Option 1 does not address the issue of the excessive tidal volume and airway pressure.
The rise in airway pressure that triggered the alarm was predictable following the increase in PEEP level (see
equation of motion). There is thus no need for 2 and 3.
Tidal volume is never titrated to an arbitrary set alarm pressure.
Pplat, which tracks alveolar pressure and the risk of developing ventilator-induced lung injury (VILI), is an easy
and accessible bedside parameter used to assess the risk of alveolar overdistension. In this patient, it is the high
Pplat associated with the choice of an excessive tidal volume that puts the patient at risk of VILI.
• Patients with ARDS have reduced aerated lung volume (“baby lungs”) and need to ventilated with small tidal
volumes: e.g., 6 ml/kg predicted ideal body weight. This patient is clearly ventilated with an excessive tidal
volume for his size (ideal or predicted body weight). The tidal volume must be reduced. A tidal volume and PEEP
combination associated with a Pplat of less than 25 cmH
2
O is generally considered safe. Concerns regarding the
risk of overdistension and VILI is significant when Pplat is > 30 cmH
2
O.
• Remember, however, that the actual distending alveolar pressure is the transpulmonary pressure (Pplat-
Ppleural). Higher Pplat can be accepted in a patient with low chest wall compliance, as less alveolar distension
will be present for the same Pplat, everything else being equal.
Sarvodaya Manav Seva Charitable Trust

41. Case 2Case 2
67-year-old female (weight 50 kg) with severe emphysema is admitted for
COPD decompensation. She failed NIPPV and required sedation, paralysis,
and intubation.
Soon after intubation and initiation of mechanical ventilation, she became
hypotensive (BP dropped from 170/95 to 80/60). She has cold extremities,
distended neck veins, midline trachea, distant heart sounds, and
symmetrical breath sounds with prolonged expiratory phase.
•Ventilatory settings are: assist control, tidal volume 500ml, rate 15/min,
PEEP 5 cmH
2
O, FIO
2
1.0 (100%)
•ABG: pH 7.20, PaO
2
250 mmHg, PaCO
2
77 mmHg
•Measured variables: rate 15/min, VE = 7.5 l/min, Ppeak 45 cmH
2
O, Pplat 30
cmH
2
O
Sarvodaya Manav Seva Charitable Trust

42. Question 1Question 1
The next step in this patient’s management should be:
–Order a stat echocardiogram to assess for tamponade.
–Order a stat AngioCT to assess for pulmonary embolism.
–Measure AutoPEEP, disconnect the patient briefly from the ventilator, then
resume ventilation with a lower tidal volume and rate and administer
intravenous fluid.
–Start the patient on intravenous dopamine and adjust the ventilator to
normalize the PaCO
2
.
Sarvodaya Manav Seva Charitable Trust

43. Answer 1Answer 1
The correct answer is 3. Remember that gas trapping is your key concern in the ventilated
patient with obstructive physiology.
• A quick look at the expiratory flow tracing and performing an expiratory pause maneuver
demonstrated that the patient has developed severe dynamic hyperinflation and intrinsic
PEEP (15 cmH
2
O).
Brief disconnection (1 - 2 minutes) from the ventilator while continuously monitoring oxygen
saturation is safe in this condition and allows for the lung to empty, intrinsic PEEP to
decrease--thus restoring venous return, preload, stroke volume, and BP. The restoration of
BP following ventilator disconnection is not specific for air trapping. Therefore, intrinsic PEEP
needs to be measured to confirm the diagnosis.
It is also important to consider the possibility of a tension pneumothorax in this patient. The
symmetrical chest and midline trachea did not suggest this possibility here.
• Also notice that Pplat was elevated (due to gas trapping), but in contrast to a patient with
stiff lungs (ARDS), there is a large difference between Ppeak and Pplat because airway
resistance is markedly elevated in patients with COPD.
Sarvodaya Manav Seva Charitable Trust

44. Question 2Question 2
•You change the ventilator’s tidal volume to 300 ml and the rate to
15/min. After 1 liter of physiologic saline is infused, the BP is now
100/70 mmHg and heart rate is 120/min. ABG: pH 7.30, PaO
2
250
mmHg, PaCO
2
60 mmHg. Measured variables: rate 20/min, VE = 6.0
l/min, Ppeak 37 cmH
2
O, Pplat 25 cmH
2
O, Intrinsic PEEP is now
7cmH
2
O (total PEEP=12 cmH
2
O).
The best next step is to:
● Continue with bronchodilators and tolerate the current mild respiratory
acidosis.
● Increase the rate to normalize PaCO
2.
● Increase the tidal volume but only to normalize the pH.
● Ask for another ABG since you do not believe the drop in PaCO
2
--minute
ventilation declined.
Sarvodaya Manav Seva Charitable Trust

45. Answer 2Answer 2
The best next step is continue with bronchodilator and
tolerate the current mild respiratory acidosis (RA).
●
The patient has no contraindications to mild RA (history of an acute or
chronic central nervous system problem, that may be worsened by the
increase in intracranial pressure associated with RA, heart failure, cardiac
ischemia, or arrhythmia.
●
Although less than present initially, dynamic hyperinflation is still an issue
(high Pplat and relatively low BP). Thus, increasing the minute ventilation to
normalize the pH or PaCO
2 will make this worse.
● The reduction in PaCO
2
is due to less air trapping, with improved venous
return and reduced dead space ventilation. Hyperinflation tends to compress
capillaries and thus promote ventilation of unperfused alveolar units (dead
space).
Sarvodaya Manav Seva Charitable Trust

46. Share the knowledge! Spread
the Health!
PLEASE SEND US THE PRESENTATIONS (PPT), DOC FILES, PDF
FILES WHICH ARE RELATED TO HEALTH & MEDICAL. WE WILL
SHOW THEM AT www.YouNHealth.Com WITH YOUR NAME.
Sarvodaya Manav Seva Charitable Trust
Email: [email protected],